Literature DB >> 16418216

Combined analysis of six lipoprotein lipase genetic variants on triglycerides, high-density lipoprotein, and ischemic heart disease: cross-sectional, prospective, and case-control studies from the Copenhagen City Heart Study.

Hans H Wittrup1, Rolf V Andersen, Anne Tybjaerg-Hansen, Gorm B Jensen, Børge G Nordestgaard.   

Abstract

CONTEXT: Genetic variants in lipoprotein lipase may affect triglycerides, high-density lipoprotein (HDL), and risk of ischemic heart disease (IHD).
OBJECTIVE: The objective of this study was to investigate the influence of T(-93)G, G(-53)C, Asp9Asn, Gly188Glu, Asn291Ser, and Ser447Ter lipoprotein lipase genotypes on triglycerides, HDL, and IHD.
DESIGN: The cross-sectional study involved 9004 adults. The prospective study consisted of 8817 adults developing 1001 IHD events over 23 yr. The case-control study involved 7818 non-IHD individuals vs. cohorts of 915 and 1062 IHD patients, respectively.
SETTING: The study was performed in the Danish general population (the Copenhagen City Heart Study). PARTICIPANTS: IHD was angina pectoris or myocardial infarction. MAIN OUTCOME MEASURES: Triglycerides, HDL, and IHD were the main outcome measures.
RESULTS: Cross-sectionally, triglycerides varied by genotype with 1.27 mmol/liter in women and 1.22 mmol/liter in men. HDL cholesterol varied by genotype with 0.49 mmol/liter in women and 0.60 mmol/liter in men. Prospectively, 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers had a hazard ratio for IHD of 1.6 [95% confidence interval (CI), 1.2-2.3]; 291Ser and 447Ter did not change IHD risk. In the case-control study, combining the cohorts of IHD patients, 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers had an odds ratio for IHD of 1.5 (CI, 1.2-2.1). 291Ser and 447Ter did not change IHD risk. Stratified for apolipoprotein E genotype, the odds ratios for IHD in 9Asn (with -93G) heterozygotes and homozygotes combined vs. noncarriers were 2.6 (CI, 1.2-5.5) among epsilon32 individuals and 2.4 (CI, 1.4-4.1) among epsilon43 individuals.
CONCLUSIONS: Genetic variation in lipoprotein lipase is associated with differences in plasma triglycerides greater than 1 mmol/liter and differences in HDL cholesterol greater than 0.5 mmol/liter. A 1.6-fold risk of IHD in 9Asn (with -93G) heterozygotes and homozygotes combined is influenced by apolipoprotein E genotype.

Entities:  

Mesh:

Substances:

Year:  2006        PMID: 16418216     DOI: 10.1210/jc.2005-1725

Source DB:  PubMed          Journal:  J Clin Endocrinol Metab        ISSN: 0021-972X            Impact factor:   5.958


  8 in total

1.  Clan genomics and the complex architecture of human disease.

Authors:  James R Lupski; John W Belmont; Eric Boerwinkle; Richard A Gibbs
Journal:  Cell       Date:  2011-09-30       Impact factor: 41.582

Review 2.  Genetic causes of high and low serum HDL-cholesterol.

Authors:  Daphna Weissglas-Volkov; Päivi Pajukanta
Journal:  J Lipid Res       Date:  2010-04-26       Impact factor: 5.922

3.  A gene score of nine LDL and HDL regulating genes is associated with fluvastatin-induced cholesterol changes in women.

Authors:  Viktor Hamrefors; Marju Orho-Melander; Ronald M Krauss; Bo Hedblad; Peter Almgren; Göran Berglund; Olle Melander
Journal:  J Lipid Res       Date:  2009-09-22       Impact factor: 5.922

4.  Additive effects of LPL, APOA5 and APOE variant combinations on triglyceride levels and hypertriglyceridemia: results of the ICARIA genetic sub-study.

Authors:  María-José Ariza; Miguel-Angel Sánchez-Chaparro; Francisco-Javier Barón; Ana-María Hornos; Eva Calvo-Bonacho; José Rioja; Pedro Valdivielso; José-Antonio Gelpi; Pedro González-Santos
Journal:  BMC Med Genet       Date:  2010-04-29       Impact factor: 2.103

5.  Food patterns associated with blood lipids are predictive of coronary heart disease: the Whitehall II study.

Authors:  Sarah A McNaughton; Gita D Mishra; Eric J Brunner
Journal:  Br J Nutr       Date:  2009-03-30       Impact factor: 3.718

6.  Modifications to the Patient Rule-Induction Method that utilize non-additive combinations of genetic and environmental effects to define partitions that predict ischemic heart disease.

Authors:  Greg Dyson; Ruth Frikke-Schmidt; Børge G Nordestgaard; Anne Tybjaerg-Hansen; Charles F Sing
Journal:  Genet Epidemiol       Date:  2009-05       Impact factor: 2.135

7.  Global O-GlcNAc Levels Modulate Transcription of the Adipocyte Secretome during Chronic Insulin Resistance.

Authors:  Edith E Wollaston-Hayden; Ruth B S Harris; Bingqiang Liu; Robert Bridger; Ying Xu; Lance Wells
Journal:  Front Endocrinol (Lausanne)       Date:  2015-01-22       Impact factor: 5.555

8.  Disparities in allele frequencies and population differentiation for 101 disease-associated single nucleotide polymorphisms between Puerto Ricans and non-Hispanic whites.

Authors:  Josiemer Mattei; Laurence D Parnell; Chao-Qiang Lai; Bibiana Garcia-Bailo; Xian Adiconis; Jian Shen; Donna Arnett; Serkalem Demissie; Katherine L Tucker; Jose M Ordovas
Journal:  BMC Genet       Date:  2009-08-14       Impact factor: 2.797

  8 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.